Interleukin-13/interleukin-4 receptor pathway is crucial for production of Sda-sialomucin in mouse small intestinal mucosa by Nippostrongylus brasiliensis infection

- Sda-sialomucins increase in mouse intestinal mucosa after N. brasiliensis infection.
- The increase in Sda-sialomucins was suppressed in IL-4Rα−/− and SCID mice.
- The expression of Sda-glycans was abrogated in IL-4Rα−/− and SCID mice.
- Administration of IL-13 led to expression of Sda-glycan in infected SCID mice.
- IL-13/IL-4R axis is important for Sda-sialomucin production during infection.

Mucin is a major component of mucus in gastrointestinal mucosa. Increase of specific sialomucins having Sda blood group antigen, NeuAcα2-3(GalNAcβ1-4)Galβ1-4GlcNAcβ-, is considered to be associated with expulsion of the parasitic intestinal nematode Nippostrongylus brasiliensis. In this study, we examined the relationship between interleukin (IL)-13 pathway and expression of Sda-sialomucins in small intestinal mucosa with N. brasiliensis infection. Nematode infection induced marked increases in small intestinal mucins that reacted with anti-Sda antibody in wild type (wt) mice. However, this increase due to infection was supressed in IL-4 receptor α deficient (IL-4Rα−/−) mice, which lack both IL-4 and IL-13 signaling via IL-4R, and severe combined immunodeficient (SCID) mice, which have defects in B- and T-lymphocytes. Analysis using tandem mass spectroscopy showed that Sda-glycans were not expressed in small intestinal mucins in IL-4Rα−/− and SCID mice after infection despite the appearance of Sda-glycans in the infected wt mice. Inoculation of recombinant IL-13 into the infected SCID mice restored expression of Sda-glycan. Our results suggest that the IL-13/IL-4R axis is important for the production of Sda-sialomucins in the host intestinal mucosa with parasitic nematode infection.

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